We write to inform the research community that a valuable collection of pancreas images, captured from autopsy samples recovered from children with recent-onset type 1 diabetes (T1D) and originally stained ∼40 years ago (1), is now available via Pancreatlas (https://pancreatlas.org/), hosted by the Vanderbilt University Medical Center. This is significant because, more than a century after the landmark discovery of insulin, the etiology of T1D in humans remains shrouded in mystery and targeted prevention of the disease in susceptible individuals is an unfulfilled objective. This largely reflects the fact that the primary sites of tissue damage (the β-cells within the islets of Langerhans in the pancreas) are not accessible by noninvasive methods at sufficiently high resolution in living subjects.
Given this limitation, much effort has been channeled into detailed analysis of T1D pancreatic tissue recovered at autopsy or made available via organ donation. Among the most valuable collections of such human pancreatic samples are those held within the contemporary Network for Pancreatic Organ Donors biobank (https://www.jdrfnpod.org/) and an archive compiled by Professor Alan Foulis in the 1980s that contains samples from many cases with an early age at onset (1). Foulis was captivated by the notion that among the residual pancreas specimens held in pathology departments across the U.K. would be autopsy samples recovered from children who had died at, or very soon after, the onset of type 1 diabetes. He understood that such pancreas specimens were likely to be linked only by a passing citation to “diabetes” on the death certificate and that they would not be cataloged in any systematic way. Undeterred, Foulis set out to access and to scrutinize relevant death certificates issued in the cases of young people dying up to the age of ∼20 years in hospitals across the U.K. between about 1950 and 1980. His laborious search ultimately yielded a list of locations from which suitable pancreas samples might be sought (1).
The ensuing collection compiled by Foulis remains unique in size and scope and comprises ∼170 fixed, paraffin-embedded pancreas tissue samples recovered at autopsy from children as young as a few months of age to those in their teens and twenties at the time of death. The majority died in ketoacidosis, and the samples ranged from a few cut sections to small tissue blocks recovered from unspecified regions of the gland. Since 2016 (on the retirement of Professor Foulis) this collection has been managed and curated by the University of Exeter Medical School as the Exeter Archival Diabetes Biobank (EADB).
From this description, there might be a temptation to conclude that the EADB represents an inauspicious historical resource with very limited contemporary scientific value. However, precisely the converse is true, and, when collecting the specimens, Foulis was intent on maximizing their use to shed new light on the underlying etiology of T1D. His goal motivates this letter, since the sections have now been scanned in digital format in collaboration with Professor Peter In’t Veld (Brussels) and are searchable using a standard set of descriptive metadata fields developed by the team at Vanderbilt. The collection is hosted in Pancreatlas (2) alongside other critically important pancreas samples, such as data and images from the Human Pancreas Analysis Program (https://hpap.pmacs.upenn.edu/). This important development now realizes the firm desire expressed by Foulis to share and promote the reuse of his carefully collected samples.
As an indication of the importance of the EADB as a resource that has illuminated the current understanding of T1D etiology, we draw attention to highly cited studies that have emerged from collaborative study of these samples (reviewed in Morgan and Richardson ). These include, as examples, the characteristics of the islet infiltrates during insulitis and islet cell hyperexpression of class I MHC, now accepted as a hallmark feature of type 1 diabetes (3). Most recently, study of these samples has also resulted in the description of disease endotypes based on immune cell profiling, which correlates with age at diagnosis (4). Such studies have complemented and extended the earlier elegant work of Gepts (5), and together they have provided important foundations on which much of our current understanding of the pancreatic immunopathology of type 1 diabetes is based.
In drawing attention to this new web interface, we also welcome inquiries from potential collaborators seeking to access the EADB as a T1D resource, especially by the application of new technologies. In doing so, we believe that the foresight shown by Foulis in compiling the collection can be expected to continue to deliver abundant dividends, as befits “a gift that keeps on giving.”
Funding. Funding for recent work undertaken with the EADB has been provided by Diabetes UK (project grant 16/0005480) and JDRF (2-SRA-2018-474-S-B).
Duality of Interest. No potential conflicts of interest relevant to this article were reported.
Author Contributions. S.J.R. and D.A.C. formatted and uploaded data, N.G.M. drafted the text, and all authors edited the manuscript for submission. N.G.M. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.